Hypertonic nacl enhances adenosine release and hormonal camp
production in mouse thick ascending limb.
Baudouin-Legros, Maryvonne, Abdallah Badou, Marc Paulais,
Mich[grave]ele Hammet, and Jacques Teulon.
INSERM U323, Facult[acute]e de M[acute]edecine Necker-Enfants
Malades, 156 rue de Vaugirard, 75015 PARIS FRANCE, Phone: 1 40 61 56
22; Fax: 1 40 61 55 91
APStracts 2:0027F, 1995.
Cyclic AMP (cAMP) accumulated in the presence of adenosine was
measured in medullary portions of mouse thick ascending limbs of
Henle's loop (mTAL) suspended either in classical extracellular
buffer, or in the presence of added NaCl. Under control conditions
(NaCl:140 mmol/l), adenosine (<10-5 mol/l) and CHA (N6
-cyclohexyladenosine, an A1 adenosine receptor agonist) inhibit the
cAMP accumulation induced by arginine-vasopressin (AVP). On the other
hand, high concentrations of adenosine and CGS21680 (2
-[p(carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine, an A2
adenosine receptor agonist) stimulate cAMP formation. Addition of
NaCl (+ 300 mmol/l) to extracellular buffer stimulates the release of
endogenous adenosine. It also enhances A2R-induced cAMP accumulation
but suppresses A1R-mediated inhibition of adenylyl cyclase. This
hypertonic NaCl medium also potentiates the stimulatory action of
arginine-vasopressin on adenylyl cyclase. The modifications of
tubular responses to both AVP and A1 and A2 agonists brought about by
hypertonic NaCl were all inhibited by adenosine deaminase, thereby
demonstrating the involvement of endogenous adenosine. Adenosine, the
release and the effects of which are modulated by hypertonic NaCl,
thus appears to act as an endogenous physiological modulator of
kidney medulla function.
Received 28 July 1994; accepted in final form 21 February 1995.
APS Manuscript Number F264-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.